Oncogenes are genes that function abnormally and help cause cancer. Oncogenes are inherited in a nononcogene form known as a protooncogene and require a triggering event to start abnormal activity. This event could be a mutation that occurs in the protooncogene itself within a single cell during mitosis. It could also be due to a more complicated chromosome abnormality occurring during mitosis in which the protooncogene is relocated in some area that promotes the oncogenic potential of the protooncogene (e.g., the abl protooncogene on chromosome 9 that is translocated to chromosome 22 and helps form the Philadelphia chromosome oncogene of CML. Another possibility is cell injury from a variety of causes such as radiation. Most of the oncogenes, when active, increase cell proliferation and thereby the number of cells with the oncogene (oncogenic “amplification”) increasing oncogene products (“overexpression”) leading to or causing carcinogenesis. Some oncogenes are actually oncogene suppressors before becoming oncogenes. If the suppressor protooncogene is deleted, damaged, or mutated on one or on both chromosomes (depending on the particular gene), the nonsuppressor oncogene (if activated as described above) is released from inhibition. The abnormal suppressor gene may even produce abnormal gene products that are synergistic to the other oncogene’s effect (e.g., the p53 suppressor protooncogene). There are many protooncogenes and oncogenes, and more are discovered every year. Some of the current most important are listed in Table 33-5. Of these, the Rb, p53, FAP, DCC, wt, and nf-1 genes are suppressors.

Some currently important oncogenes

Table 33-5 Some currently important oncogenes